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{{short description|Small projection on a neuron that receive signals}}

Certain classes of dendrites contain small projections referred to as dendritic spines that increase receptive properties of dendrites to isolate signal specificity. Increased neural activity and the establishment of long-term potentiation at dendritic spines change the sizes, shape, and conduction. This ability for dendritic growth is thought to play a role in learning and memory formation. There can be as many as 15,000 spines per cell, each of which serves as a postsynaptic process for individual presynaptic axons. Dendritic branching can be extensive and in some cases is sufficient to receive as many as 100,000 inputs to a single neuron. Dendrites are one of two types of protoplasmic protrusions that extrude from the cell body of a neuron, the other type being an axon. Axons can be distinguished from dendrites by several features including shape, length, and function. Dendrites often taper off in shape and are shorter, while axons tend to maintain a constant radius and be relatively long. Typically, axons transmit electrochemical signals and dendrites receive the electrochemical signals, although some types of neurons in certain species lack axons and simply transmit signals via their dendrites. Dendrites provide an enlarged surface area to receive signals from the terminal buttons of other axons, and the axon also commonly divides at its far end into many branches (telodendria) each of which ends in a nerve terminal, allowing a chemical signal to pass simultaneously to many target cells.

{{Redirect|Dendritic branch|the dendritic cell of the immune system|Dendritic cell}}

{{About|neuronal dendrites in biology}}

'''Dendrites''' (from [[Ancient Greek language|Greek]] δένδρον ''déndron'', "tree"), also '''dendrons''', are branched protoplasmic extensions of a nerve cell that propagate the [[neurotransmission|electrochemical stimulation]] received from other neural cells to the cell body, or [[Soma (biology)|soma]], of the [[neuron]] from which the dendrites project. Electrical stimulation is transmitted onto dendrites by upstream neurons (usually via their [[axon]]s) via [[synapses]] which are located at various points throughout the dendritic tree. Dendrites play a critical role in integrating these [[synapse|synaptic inputs]] and in determining the extent to which [[action potentials]] are produced by the neuron.<ref name="urbanska" /> '''Dendritic arborization'''<!--term redirects here: bolded per MOS:BOLD-->, also known as '''dendritic branching''', is a multi-step biological process by which neurons form new [[dendritic tree]]s and branches to create new synapses.<ref name=urbanska /> The [[Morphology (biology)|morphology]] of dendrites such as branch density and grouping patterns are highly correlated to the function of the neuron. Malformation of dendrites is also tightly correlated to impaired nervous system function.<ref name=Tavosanis /> Some disorders that are associated with the malformation of dendrites are autism, depression, schizophrenia, Down syndrome and anxiety.{{Citation needed|date=October 2021}}

Typically, when an electrochemical signal stimulates a neuron, it occurs at a dendrite and causes changes in the electrical potential across the neuron's plasma membrane. This change in the membrane potential will passively spread across the dendrite but becomes weaker with distance without an action potential. An action potential propagates the electrical activity along the membrane of the neuron's dendrites to the cell body and then afferently down the length of the axon to the axon terminal, where it triggers the release of neurotransmitters into the synaptic cleft. However, synapses involving dendrites can also be axodendritic, involving an axon signaling to a dendrite, or dendrodendritic, involving signaling between dendrites. An autapse is a synapse in which the axon of one neuron transmits signals to its own dendrites.[[File:Dendrites of neural tissue.jpg|thumb|The green arrow shows the dendrites emanating from soma|链接=Special:FilePath/Dendrites_of_neural_tissue.jpg]]

某些类型的树突具有称为树突棘的小突起，增加树突的信号接收特性，通过隔离增强信号的特异性。树突棘的神经活动增强和长时程增强会改变其大小、形状和传导性能。这种树突生长能力被认为在学习和记忆形成中起着重要作用。每个细胞可以有多达 15,000 个树突棘，每个都可以作为单个突触前轴突的突触后突起<ref>{{cite journal|last=Koch|first=C.|author2=Zador, A.|title=The Function of Dendritic Spines: Devices Subserving Biochemical Rather Than Electrical Compartmentalization|journal=The Journal of Neuroscience|date=February 1993|volume=13|issue=2|pages=413–422|pmid=8426220|pmc=6576662|doi=10.1523/JNEUROSCI.13-02-00413.1993}}</ref>。树突分支可以非常庞大，足以为单个神经元接收多达 100,000 个输入<ref name="Alberts 2009">{{cite book|last=Alberts|first=Bruce|title=Essential Cell Biology|date=2009|publisher=Garland Science|location=New York|isbn=978-0-8153-4129-1|edition=3rd}}</ref>。树突是从神经元细胞体延伸出来的两种原生质突起之一，另一种是轴突。轴突与树突可以通过几个特征来区分，包括形状、长度和功能。树突有逐渐变细的形状，更短，而轴突倾向于保持恒定的半径，相对较长。通常，轴突传递电化学信号，树突接收电化学信号，尽管某些种类的神经元没有轴突，仅仅通过树突传递信号<ref name="Yau" /> 。树突提供了扩大的表面区域来接收来自其他轴突末端的信号，轴突也通常在其远端形成许多分支（终树突），每个分支形成一个神经末梢，允许一种化学信号同时传递给许多目标细胞<ref name="Alberts 2009" /> 。当电化学信号，通常在树突部位，刺激神经元，并引起神经元质膜电位的变化。这种膜电位的变化会在整个树突进行被动扩布，但随着距离的增加而变弱，不会产生动作电位。动作电位沿着神经元树突的细胞膜传递电活动到胞体，然后沿着轴突传递到轴突末梢，在那里触发神经递质的释放到突触间隙<ref name="Alberts 2009" />。然而，包含树突的突触也可以是轴树突触，即从轴突向树突传递信号，也可以是树树突触，即树突之间传递信号<ref name="Carlson 2013">{{cite book|last=Carlson|first=Neil R.|title=Physiology of Behavior|date=2013|publisher=Pearson|location=Boston|isbn=978-0-205-23939-9|edition=11th}}</ref>。自突触是一种神经元的轴突将信号传递给自身树突的突触。

There are three main types of neurons; multipolar, bipolar, and unipolar. Multipolar neurons, such as the one shown in the image, are composed of one axon and many dendritic trees. Pyramidal cells are multipolar cortical neurons with pyramid shaped cell bodies and large dendrites called [[apical dendrite]]s that extend to the surface of the cortex. Bipolar neurons have one axon and one dendritic tree at opposing ends of the cell body. Unipolar neurons have a stalk that extends from the cell body that separates into two branches with one containing the dendrites and the other with the terminal buttons. Unipolar dendrites are used to detect sensory stimuli such as touch or temperature.<ref name="Carlson 2013" /><ref>{{cite book|last=Pinel|first=John P.J.|title=Biopsychology|date=2011|publisher=Allyn & Bacon|location=Boston|isbn=978-0-205-83256-9|edition=8th}}</ref><ref>{{Cite journal | last1 = Jan | first1 = Y. N. | last2 = Jan | first2 = L. Y. | doi = 10.1038/nrn2836 | title = Branching out: Mechanisms of dendritic arborization | journal = Nature Reviews Neuroscience | volume = 11 | issue = 5 | pages = 316–328 | year = 2010 | pmid = 20404840 | pmc =3079328 }}</ref>

 

 

 

 

 

There are three main types of neurons; multipolar, bipolar, and unipolar. Multipolar neurons, such as the one shown in the image, are composed of one axon and many dendritic trees. Pyramidal cells are multipolar cortical neurons with pyramid shaped cell bodies and large dendrites called [[apical dendrite]]s that extend to the surface of the cortex. Bipolar neurons have one axon and one dendritic tree at opposing ends of the cell body. Unipolar neurons have a stalk that extends from the cell body that separates into two branches with one containing the dendrites and the other with the terminal buttons. Unipolar dendrites are used to detect sensory stimuli such as touch or temperature.<ref name="Carlson 2013"/><ref>{{cite book|last=Pinel|first=John P.J.|title=Biopsychology|date=2011|publisher=Allyn & Bacon|location=Boston|isbn=978-0-205-83256-9|edition=8th}}</ref><ref>{{Cite journal | last1 = Jan | first1 = Y. N. | last2 = Jan | first2 = L. Y. | doi = 10.1038/nrn2836 | title = Branching out: Mechanisms of dendritic arborization | journal = Nature Reviews Neuroscience | volume = 11 | issue = 5 | pages = 316–328 | year = 2010 | pmid = 20404840 | pmc =3079328 }}</ref>

There are three main types of neurons; multipolar, bipolar, and unipolar. Multipolar neurons, such as the one shown in the image, are composed of one axon and many dendritic trees. Pyramidal cells are multipolar cortical neurons with pyramid shaped cell bodies and large dendrites called apical dendrites that extend to the surface of the cortex. Bipolar neurons have one axon and one dendritic tree at opposing ends of the cell body. Unipolar neurons have a stalk that extends from the cell body that separates into two branches with one containing the dendrites and the other with the terminal buttons. Unipolar dendrites are used to detect sensory stimuli such as touch or temperature.

There are three main types of neurons; multipolar, bipolar, and unipolar. Multipolar neurons, such as the one shown in the image, are composed of one axon and many dendritic trees. Pyramidal cells are multipolar cortical neurons with pyramid shaped cell bodies and large dendrites called apical dendrites that extend to the surface of the cortex. Bipolar neurons have one axon and one dendritic tree at opposing ends of the cell body. Unipolar neurons have a stalk that extends from the cell body that separates into two branches with one containing the dendrites and the other with the terminal buttons. Unipolar dendrites are used to detect sensory stimuli such as touch or temperature.

==History==

==历史==

The term ''dendrites'' was first used in 1889 by [[Wilhelm His, Sr.|Wilhelm His]] to describe the number of smaller "protoplasmic processes" that were attached to a [[Neuron|nerve cell]].<ref>{{Cite book|title=Origins of neuroscience : a history of explorations into brain function|last=Finger|first=Stanley|publisher=Oxford University Press|year=1994|isbn=9780195146943|pages=44|oclc=27151391|quote=The nerve cell with its uninterrupted processes was described by Otto Friedrich Karl Deiters (1834-1863) in a work that was completed by Max Schultze (1825-1874) in 1865, two years after Deiters died of typhoid fever. This work portrayed the cell body with a single chief "axis cylinder" and a number of smaller "protoplasmic processes" (see figure 3.19). The latter would become known as "dendrites", a term coined by Wilhelm His (1831-1904) in 1889.}}</ref> German anatomist [[Otto Friedrich Karl Deiters]] is generally credited with the discovery of the axon by distinguishing it from the dendrites.

The term ''dendrites'' was first used in 1889 by [[Wilhelm His, Sr.|Wilhelm His]] to describe the number of smaller "protoplasmic processes" that were attached to a [[Neuron|nerve cell]].<ref>{{Cite book|title=Origins of neuroscience : a history of explorations into brain function|last=Finger|first=Stanley|publisher=Oxford University Press|year=1994|isbn=9780195146943|pages=44|oclc=27151391|quote=The nerve cell with its uninterrupted processes was described by Otto Friedrich Karl Deiters (1834-1863) in a work that was completed by Max Schultze (1825-1874) in 1865, two years after Deiters died of typhoid fever. This work portrayed the cell body with a single chief "axis cylinder" and a number of smaller "protoplasmic processes" (see figure 3.19). The latter would become known as "dendrites", a term coined by Wilhelm His (1831-1904) in 1889.}}</ref> German anatomist [[Otto Friedrich Karl Deiters]] is generally credited with the discovery of the axon by distinguishing it from the dendrites.

The term dendrites was first used in 1889 by Wilhelm His to describe the number of smaller "protoplasmic processes" that were attached to a nerve cell. German anatomist Otto Friedrich Karl Deiters is generally credited with the discovery of the axon by distinguishing it from the dendrites.

The term dendrites was first used in 1889 by Wilhelm His to describe the number of smaller "protoplasmic processes" that were attached to a nerve cell. German anatomist Otto Friedrich Karl Deiters is generally credited with the discovery of the axon by distinguishing it from the dendrites.

树突（''dendrite''）这一术语最早是在 1889 年被 [[Wilhelm His, Sr.|Wilhelm His]] 用来描述神经细胞相连的较小的“原生质突起”的数量。德国解剖学家 [[Otto Friedrich Karl Deiters]] 被认为发现了轴突，是他首先将轴突与树突区分开。

 

Some of the first intracellular recordings in a nervous system were made in the late 1930s by [[Kenneth S. Cole]] and Howard J. Curtis. Swiss Rüdolf Albert von Kölliker and German Robert Remak were the first to identify and characterize the [[axonal initial segment]]. [[Alan Hodgkin]] and [[Andrew Huxley]] also employed the [[squid giant axon]] (1939) and by 1952 they had obtained a full quantitative description of the ionic basis of the [[action potential]], leading the formulation of the [[Hodgkin–Huxley model]]. Hodgkin and Huxley were awarded jointly the [[Nobel Prize]] for this work in 1963. The formulas detailing axonal conductance were extended to vertebrates in the Frankenhaeuser–Huxley equations. Louis-Antoine Ranvier was the first to describe the gaps or nodes found on axons and for this contribution these axonal features are now commonly referred to as the Nodes of Ranvier. Santiago Ramón y Cajal, a Spanish anatomist, proposed that axons were the output components of neurons.<ref>{{cite journal|last=Debanne|first=D|author2=Campanac, E |author3=Bialowas, A |author4=Carlier, E |author5= Alcaraz, G |title=Axon physiology.|journal=Physiological Reviews|date=Apr 2011|volume=91|issue=2|pages=555–602|pmid=21527732 |doi=10.1152/physrev.00048.2009|url=https://hal-amu.archives-ouvertes.fr/hal-01766861/file/Debanne-Physiol-Rev-2011.pdf}}</ref> He also proposed that [[neurons]] were discrete cells that communicated with each other via specialized junctions, or spaces, between cells, now known as a [[synapse]]. Ramón y Cajal improved a silver staining process known as Golgi's method, which had been developed by his rival, [[Camillo Golgi]].<ref>{{cite journal|last=López-Muñoz|first=F|title=Neuron theory, the cornerstone of neuroscience, on the centenary of the Nobel Prize award to Santiago Ramón y Cajal|journal=Brain Research Bulletin|volume=70|issue=4–6|pages=391–405|pmid=17027775|doi=10.1016/j.brainresbull.2006.07.010|date=October 2006|s2cid=11273256}}</ref>

Some of the first intracellular recordings in a nervous system were made in the late 1930s by Kenneth S. Cole and Howard J. Curtis. Swiss Rüdolf Albert von Kölliker and German Robert Remak were the first to identify and characterize the axonal initial segment. Alan Hodgkin and Andrew Huxley also employed the squid giant axon (1939) and by 1952 they had obtained a full quantitative description of the ionic basis of the action potential, leading the formulation of the Hodgkin–Huxley model. Hodgkin and Huxley were awarded jointly the Nobel Prize for this work in 1963. The formulas detailing axonal conductance were extended to vertebrates in the Frankenhaeuser–Huxley equations. Louis-Antoine Ranvier was the first to describe the gaps or nodes found on axons and for this contribution these axonal features are now commonly referred to as the Nodes of Ranvier. Santiago Ramón y Cajal, a Spanish anatomist, proposed that axons were the output components of neurons. He also proposed that neurons were discrete cells that communicated with each other via specialized junctions, or spaces, between cells, now known as a synapse. Ramón y Cajal improved a silver staining process known as Golgi's method, which had been developed by his rival, Camillo Golgi.

Some of the first intracellular recordings in a nervous system were made in the late 1930s by Kenneth S. Cole and Howard J. Curtis. Swiss Rüdolf Albert von Kölliker and German Robert Remak were the first to identify and characterize the axonal initial segment. Alan Hodgkin and Andrew Huxley also employed the squid giant axon (1939) and by 1952 they had obtained a full quantitative description of the ionic basis of the action potential, leading the formulation of the Hodgkin–Huxley model. Hodgkin and Huxley were awarded jointly the Nobel Prize for this work in 1963. The formulas detailing axonal conductance were extended to vertebrates in the Frankenhaeuser–Huxley equations. Louis-Antoine Ranvier was the first to describe the gaps or nodes found on axons and for this contribution these axonal features are now commonly referred to as the Nodes of Ranvier. Santiago Ramón y Cajal, a Spanish anatomist, proposed that axons were the output components of neurons. He also proposed that neurons were discrete cells that communicated with each other via specialized junctions, or spaces, between cells, now known as a synapse. Ramón y Cajal improved a silver staining process known as Golgi's method, which had been developed by his rival, Camillo Golgi.

上世纪30年代末，肯尼斯 · s · 科尔和霍华德 · j · 柯蒂斯首次对神经系统进行了细胞内记录。瑞士的阿尔伯特·冯·科立克和德国的 Robert Remak 是第一个识别和描述轴突初始部分的人。1952年，他们获得了动作电位离子基础的完整定量描述，从而引导了 Hodgkin-Huxley 模型的形成。1963年，霍奇金和赫胥黎因这项工作共同获得了诺贝尔奖。在 Frankenhaeuser-Huxley 方程式中，细化轴突电导的公式被推广到脊椎动物。Louis-Antoine Ranvier 是第一个描述轴突间隙或节点的人，因此这些轴突特征现在通常被称为郎飞结。西班牙解剖学家圣地亚哥·拉蒙-卡哈尔提出轴突是神经元的输出组件。他还提出，神经元是离散的细胞，通过细胞之间的特殊连接或空间彼此沟通，现在称为突触。拉蒙 · 卡哈尔改进了他的竞争对手卡米洛 · 高尔基发明的高尔基染色法。

1930 年代末，[[Kenneth S. Cole]] 和 Howard J. Curtis 开展了最早的神经系统胞内电生理记录。瑞士人 Rüdolf Albert von Kölliker 和德国人 German Robert Remak 首先对轴突起始段进行了鉴定和性质研究。1952 年，[[Alan Hodgkin]] 和 [[Andrew Huxley]] 也使用了乌贼巨突触（1939年），到 1952 年他们得到动作电位的离子机制的完整定量描述，从而建立了 Hodgkin-Huxley 模型。Hodgkin 和 Huxley 因这项工作在 1963 年共同获得诺贝尔奖。Frankenhaeuser-Huxley 方程式则将详细描述轴突传导的公式推广到脊椎动物。Louis-Antoine Ranvier 首次描述了轴突上的不连续或饥结，因此这些轴突特征现在通常被称为郎飞结。西班牙解剖学家 Ramón y Cajal 提出轴突是神经元输出的部分<ref>{{cite journal|last=Debanne|first=D|author2=Campanac, E |author3=Bialowas, A |author4=Carlier, E |author5= Alcaraz, G |title=Axon physiology.|journal=Physiological Reviews|date=Apr 2011|volume=91|issue=2|pages=555–602|pmid=21527732 |doi=10.1152/physrev.00048.2009|url=https://hal-amu.archives-ouvertes.fr/hal-01766861/file/Debanne-Physiol-Rev-2011.pdf}}</ref>。他还提出，神经元是离散的细胞，通过细胞间的特殊连接或空隙彼此沟通，今天称为突触的结构进行相互通信。Ramón y Cajal 改进了他的竞争对手 [[Camillo Golgi]] 发明的高尔基染色法<ref>{{cite journal|last=López-Muñoz|first=F|title=Neuron theory, the cornerstone of neuroscience, on the centenary of the Nobel Prize award to Santiago Ramón y Cajal|journal=Brain Research Bulletin|volume=70|issue=4–6|pages=391–405|pmid=17027775|doi=10.1016/j.brainresbull.2006.07.010|date=October 2006|s2cid=11273256}}</ref>。

==Dendrite development==

==Dendrite development 树突发育==

[[File:Complete neuron cell diagram en.svg|thumb|right|277px]]

[[File:Complete neuron cell diagram en.svg|thumb|right|277px]]

During the development of dendrites, several factors can influence differentiation. These include modulation of sensory input, environmental pollutants, body temperature, and drug use.<ref>{{cite journal|last=McEwen|first=Bruce S.|title=Stress, sex, and neural adaptation to a changing environment: mechanisms of neuronal remodeling|journal=Annals of the New York Academy of Sciences|volume=1204|pages=38–59|doi=10.1111/j.1749-6632.2010.05568.x|year=2010|bibcode=2010NYASA1204...38M|pmid=20840167|pmc=2946089}}</ref> For example, rats raised in dark environments were found to have a reduced number of spines in pyramidal cells located in the primary visual cortex and a marked change in distribution of dendrite branching in layer 4 stellate cells.<ref>{{cite journal|last=Borges|first=S.|author2=Berry, M.|title=The effects of dark rearing on the development of the visual cortex of the rat|journal=The Journal of Comparative Neurology|date=15 July 1978|volume=180|issue=2|pages=277–300|doi=10.1002/cne.901800207|pmid=659662|s2cid=42749947}}</ref> Experiments done in vitro and in vivo have shown that the presence of afferents and input activity per se can modulate the patterns in which dendrites differentiate.<ref name=Tavosanis />

During the development of dendrites, several factors can influence differentiation. These include modulation of sensory input, environmental pollutants, body temperature, and drug use.<ref name=":0">{{cite journal|last=McEwen|first=Bruce S.|title=Stress, sex, and neural adaptation to a changing environment: mechanisms of neuronal remodeling|journal=Annals of the New York Academy of Sciences|volume=1204|pages=38–59|doi=10.1111/j.1749-6632.2010.05568.x|year=2010|bibcode=2010NYASA1204...38M|pmid=20840167|pmc=2946089}}</ref> For example, rats raised in dark environments were found to have a reduced number of spines in pyramidal cells located in the primary visual cortex and a marked change in distribution of dendrite branching in layer 4 stellate cells.<ref name=":1">{{cite journal|last=Borges|first=S.|author2=Berry, M.|title=The effects of dark rearing on the development of the visual cortex of the rat|journal=The Journal of Comparative Neurology|date=15 July 1978|volume=180|issue=2|pages=277–300|doi=10.1002/cne.901800207|pmid=659662|s2cid=42749947}}</ref> Experiments done in vitro and in vivo have shown that the presence of afferents and input activity per se can modulate the patterns in which dendrites differentiate.<ref name=Tavosanis />

在树突的发育过程中，有几个因素可以影响这种分化，包括感觉输入调控、环境污染物、体温和药物使用<ref name=":0" /> 。例如，在黑暗环境中长大的大鼠，初级视皮层的锥体细胞的树突棘数量减少，在第 4 层星状细胞中树突分支的分布有明显的不同<ref name=":1" /> 。体外和体内实验表明，传入神经和传入神经活动本身可以调节树突分化的模式<ref name="Tavosanis" />。

During the development of dendrites, several factors can influence differentiation. These include modulation of sensory input, environmental pollutants, body temperature, and drug use. For example, rats raised in dark environments were found to have a reduced number of spines in pyramidal cells located in the primary visual cortex and a marked change in distribution of dendrite branching in layer 4 stellate cells. Experiments done in vitro and in vivo have shown that the presence of afferents and input activity per se can modulate the patterns in which dendrites differentiate.

= = = 树枝晶发育 = = 拇指 | 右 | 277px 在树枝晶的发育过程中，有几个因素可以影响分化。这些包括调节感觉输入，环境污染物，体温和药物使用。例如，在黑暗环境中长大的老鼠，在初级视皮层锥体细胞中的刺数量减少，在第4层星状细胞中树突分支的分布有明显的变化。体外和体内的实验表明，传入物的存在和输入活性本身可以调节树突分化的模式。

Little is known about the process by which dendrites orient themselves in vivo and are compelled to create the intricate branching pattern unique to each specific neuronal class. One theory on the mechanism of dendritic arbor development is the Synaptotropic Hypothesis. The synaptotropic hypothesis proposes that input from a presynaptic to a postsynaptic cell (and maturation of excitatory synaptic inputs) eventually can change the course of synapse formation at dendritic and axonal arbors.<ref name=":2">{{cite journal|last=Cline|first=H|author2=Haas, K|title=The regulation of dendritic arbor development and plasticity by glutamatergic synaptic input: a review of the synaptotrophic hypothesis.|journal=The Journal of Physiology|date=Mar 15, 2008|volume=586|issue=6|pages=1509–17|pmid=18202093|doi=10.1113/jphysiol.2007.150029|pmc=2375708}}</ref> This synapse formation is required for the development of neuronal structure in the functioning brain. A balance between metabolic costs of dendritic elaboration and the need to cover receptive field presumably determine the size and shape of dendrites. A complex array of extracellular and intracellular cues modulates dendrite development including transcription factors, receptor-ligand interactions, various signaling pathways, local translational machinery, cytoskeletal elements, Golgi outposts and endosomes. These contribute to the organization of the dendrites on individual cell bodies and the placement of these dendrites in the neuronal circuitry. For example, it was shown that β-actin zipcode binding protein 1 (ZBP1) contributes to proper dendritic branching. Other important transcription factors involved in the morphology of dendrites include CUT, Abrupt, Collier, Spineless, ACJ6/drifter, CREST, NEUROD1, CREB, NEUROG2 etc. Secreted proteins and cell surface receptors includes neurotrophins and tyrosine kinase receptors, BMP7, Wnt/dishevelled, EPHB 1–3, Semaphorin/plexin-neuropilin, slit-robo, netrin-frazzled, reelin. Rac, CDC42 and RhoA serve as cytoskeletal regulators and the motor protein includes KIF5, dynein, LIS1. Important secretory and endocytic pathways controlling the dendritic development include DAR3 /SAR1, DAR2/Sec23, DAR6/Rab1 etc. All these molecules interplay with each other in controlling dendritic morphogenesis including the acquisition of type specific dendritic arborization, the regulation of dendrite size and the organization of dendrites emanating from different neurons.<ref name="urbanska" /><ref name="perycz" />

Little is known about the process by which dendrites orient themselves in vivo and are compelled to create the intricate branching pattern unique to each specific neuronal class. One theory on the mechanism of dendritic arbor development is the Synaptotropic Hypothesis. The synaptotropic hypothesis proposes that input from a presynaptic to a postsynaptic cell (and maturation of excitatory synaptic inputs) eventually can change the course of synapse formation at dendritic and axonal arbors.<ref>{{cite journal|last=Cline|first=H|author2=Haas, K|title=The regulation of dendritic arbor development and plasticity by glutamatergic synaptic input: a review of the synaptotrophic hypothesis.|journal=The Journal of Physiology|date=Mar 15, 2008|volume=586|issue=6|pages=1509–17|pmid=18202093|doi=10.1113/jphysiol.2007.150029|pmc=2375708}}</ref> This synapse formation is required for the development of neuronal structure in the functioning brain. A balance between metabolic costs of dendritic elaboration and the need to cover receptive field presumably determine the size and shape of dendrites. A complex array of extracellular and intracellular cues modulates dendrite development including transcription factors, receptor-ligand interactions, various signaling pathways, local translational machinery, cytoskeletal elements, Golgi outposts and endosomes. These contribute to the organization of the dendrites on individual cell bodies and the placement of these dendrites in the neuronal circuitry. For example, it was shown that β-actin zipcode binding protein 1 (ZBP1) contributes to proper dendritic branching. Other important transcription factors involved in the morphology of dendrites include CUT, Abrupt, Collier, Spineless, ACJ6/drifter, CREST, NEUROD1, CREB, NEUROG2 etc. Secreted proteins and cell surface receptors includes neurotrophins and tyrosine kinase receptors, BMP7, Wnt/dishevelled, EPHB 1–3, Semaphorin/plexin-neuropilin, slit-robo, netrin-frazzled, reelin. Rac, CDC42 and RhoA serve as cytoskeletal regulators and the motor protein includes KIF5, dynein, LIS1. Important secretory and endocytic pathways controlling the dendritic development include DAR3 /SAR1, DAR2/Sec23, DAR6/Rab1 etc. All these molecules interplay with each other in controlling dendritic morphogenesis including the acquisition of type specific dendritic arborization, the regulation of dendrite size and the organization of dendrites emanating from different neurons.<ref name=urbanska /><ref name=perycz />

树突如何在体内定向，并产生特定神经元类别特有的复杂分支模式，这个过程我们知之甚少。树突分支发育机制的一个理论是突触营养假设。突触营养假设认为，突触前细胞向突触后细胞的输入（以及兴奋性突触输入的成熟）最终可以改变树突和轴突末梢的分支形成突触的进程<ref name=":2" /> 。这种突触形成对工作中的大脑的神经元结构发育所必需的。树突复杂分支的形成的代谢成本和覆盖感受野的需要之间的平衡大体决定了树突的大小和形状。一系列复杂的胞外和胞内信号，包括转录因子、受体-配体相互作用、各种信号通路、局部翻译机制、细胞骨架元件、高尔基前哨和内涵体，都会调节树突发育。这些促进了单个细胞胞体上树突的组织以及这些树突在神经回路中的定位。例如，研究表明 β 肌动蛋白结合蛋白1（β-actin zipcode binding protein 1，ZBP1）在树突形成正常分支中有作用。其他与树突形态有关的重要转录因子包括 CUT、stump、Collier、Spineless、ACJ6/drifter、CREST、NEUROD1、CREB、neurog2 等。分泌蛋白和细胞表面受体包括神经营养因子和酪氨酸受体激酶、BMP7、Wnt/dishevelled、EPHB 1-3、 Semaphorin/plexin-neuropilin、slit-robo、netrin-frazzled、reelin。Rac, CDC42 和 RhoA 作为细胞骨架调节分子，马达蛋白包括 KIF5、dynein、LIS1。控制树突发育的重要分泌和内吞途径包括 DAR3/SAR1、DAR2/Sec23、DAR6/rab1 等。所有这些分子在控制树突形态发生中相互作用，包括细胞类型特异的树突分支、树突大小和不同神经元树突的组织<ref name=urbanska /><ref name=perycz />。

==Electrical properties 电性质==

 

The structure and branching of a neuron's dendrites, as well as the availability and variation of [[voltage-gated ion channel|voltage-gated ion conductance]], strongly influences how the neuron integrates the input from other neurons. This integration is both temporal, involving the summation of stimuli that arrive in rapid succession, as well as spatial, entailing the aggregation of excitatory and inhibitory inputs from separate branches.<ref name=":3">{{cite book|last=Kandel|first=Eric R.|title=Principles of neural science.|date=2003|publisher=McGrawHill|location=Cambridge|isbn=0-8385-7701-6|edition=4th|url-access=registration|url=https://archive.org/details/isbn_9780838577011}}</ref>

 

==Electrical properties==

The structure and branching of a neuron's dendrites, as well as the availability and variation of [[voltage-gated ion channel|voltage-gated ion conductance]], strongly influences how the neuron integrates the input from other neurons. This integration is both temporal, involving the summation of stimuli that arrive in rapid succession, as well as spatial, entailing the aggregation of excitatory and inhibitory inputs from separate branches.<ref>{{cite book|last=Kandel|first=Eric R.|title=Principles of neural science.|date=2003|publisher=McGrawHill|location=Cambridge|isbn=0-8385-7701-6|edition=4th|url-access=registration|url=https://archive.org/details/isbn_9780838577011}}</ref>

The structure and branching of a neuron's dendrites, as well as the availability and variation of voltage-gated ion conductance, strongly influences how the neuron integrates the input from other neurons. This integration is both temporal, involving the summation of stimuli that arrive in rapid succession, as well as spatial, entailing the aggregation of excitatory and inhibitory inputs from separate branches.

The structure and branching of a neuron's dendrites, as well as the availability and variation of voltage-gated ion conductance, strongly influences how the neuron integrates the input from other neurons. This integration is both temporal, involving the summation of stimuli that arrive in rapid succession, as well as spatial, entailing the aggregation of excitatory and inhibitory inputs from separate branches.

Dendrites were once thought to merely convey electrical stimulation passively. This passive transmission means that [[voltage]] changes measured at the cell body are the result of activation of distal synapses propagating the electric signal towards the cell body without the aid of [[voltage-gated ion channels]]. [[Cable theory|Passive cable theory]] describes how voltage changes at a particular location on a dendrite transmit this electrical signal through a system of converging dendrite segments of different diameters, lengths, and electrical properties. Based on passive cable theory one can track how changes in a neuron's dendritic morphology impacts the membrane voltage at the cell body, and thus how variation in dendrite architectures affects the overall output characteristics of the neuron.<ref name="Koch 1999">{{cite book|last=Koch|first=Christof|title=Biophysics of computation : information processing in single neurons|date=1999|publisher=Oxford Univ. Press|location=New York [u.a.]|isbn=0-19-510491-9}}</ref><ref name="Häusser 2008">{{cite book|last=Häusser|first=Michael|title=Dendrites|date=2008|publisher=Oxford University Press|location=Oxford|isbn=978-0-19-856656-4|edition=2nd}}</ref>

Dendrites were once thought to merely convey electrical stimulation passively. This passive transmission means that [[voltage]] changes measured at the cell body are the result of activation of distal synapses propagating the electric signal towards the cell body without the aid of [[voltage-gated ion channels]]. [[Cable theory|Passive cable theory]] describes how voltage changes at a particular location on a dendrite transmit this electrical signal through a system of converging dendrite segments of different diameters, lengths, and electrical properties. Based on passive cable theory one can track how changes in a neuron's dendritic morphology impacts the membrane voltage at the cell body, and thus how variation in dendrite architectures affects the overall output characteristics of the neuron.<ref name="Koch 1999">{{cite book|last=Koch|first=Christof|title=Biophysics of computation : information processing in single neurons|date=1999|publisher=Oxford Univ. Press|location=New York [u.a.]|isbn=0-19-510491-9}}</ref><ref name="Häusser 2008">{{cite book|last=Häusser|first=Michael|title=Dendrites|date=2008|publisher=Oxford University Press|location=Oxford|isbn=978-0-19-856656-4|edition=2nd}}</ref>

 

Electrochemical signals are propagated by action potentials that utilize intermembrane voltage-gated ion channels to transport sodium ions, calcium ions, and potassium ions. Each ion species has its own corresponding protein channel located in the lipid bilayer of the cell membrane. The cell membrane of neurons covers the axons, cell body, dendrites, etc. The protein channels can differ between chemical species in the amount of required activation voltage and the activation duration.<ref name="Alberts 2009"/>

Electrochemical signals are propagated by action potentials that utilize intermembrane voltage-gated ion channels to transport sodium ions, calcium ions, and potassium ions. Each ion species has its own corresponding protein channel located in the lipid bilayer of the cell membrane. The cell membrane of neurons covers the axons, cell body, dendrites, etc. The protein channels can differ between chemical species in the amount of required activation voltage and the activation duration.<ref name="Alberts 2009"/>

电化学信号可以利用动作电位进行传播，动作电位使用电压门控离子通道跨膜转运钠离子、钙离子和钾离子。每种离子在细胞膜的脂质双分子层中都有自己对应的蛋白通道。神经元的细胞膜覆盖轴突、胞体、树突等。不同离子的蛋白质通道具有不同的激活电位和持续时间<ref name="Alberts 2009" />。

 

 

Action potentials in animal cells are generated by either sodium-gated or calcium-gated ion channels in the plasma membrane. These channels are closed when the membrane potential is near to, or at, the resting potential of the cell. The channels will start to open if the membrane potential increases, allowing sodium or calcium ions to flow into the cell. As more ions enter the cell, the membrane potential continues to rise. The process continues until all of the ion channels are open, causing a rapid increase in the membrane potential that then triggers the decrease in the membrane potential. The depolarizing is caused by the closing of the ion channels that prevent sodium ions from entering the neuron, and they are then actively transported out of the cell. Potassium channels are then activated, and there is an outward flow of potassium ions, returning the electrochemical gradient to the resting potential. After an action potential has occurred, there is a transient negative shift, called the afterhyperpolarization or refractory period, due to additional potassium currents. This is the mechanism that prevents an action potential from traveling back the way it just came.<ref name="Alberts 2009"/><ref>{{cite journal|last=Barnett|first=MW|author2=Larkman, PM|title=The action potential.|journal=Practical Neurology|date=Jun 2007|volume=7|issue=3|pages=192–7|pmid=17515599}}</ref>

Action potentials in animal cells are generated by either sodium-gated or calcium-gated ion channels in the plasma membrane. These channels are closed when the membrane potential is near to, or at, the resting potential of the cell. The channels will start to open if the membrane potential increases, allowing sodium or calcium ions to flow into the cell. As more ions enter the cell, the membrane potential continues to rise. The process continues until all of the ion channels are open, causing a rapid increase in the membrane potential that then triggers the decrease in the membrane potential. The depolarizing is caused by the closing of the ion channels that prevent sodium ions from entering the neuron, and they are then actively transported out of the cell. Potassium channels are then activated, and there is an outward flow of potassium ions, returning the electrochemical gradient to the resting potential. After an action potential has occurred, there is a transient negative shift, called the afterhyperpolarization or refractory period, due to additional potassium currents. This is the mechanism that prevents an action potential from traveling back the way it just came.

Action potentials in animal cells are generated by either sodium-gated or calcium-gated ion channels in the plasma membrane. These channels are closed when the membrane potential is near to, or at, the resting potential of the cell. The channels will start to open if the membrane potential increases, allowing sodium or calcium ions to flow into the cell. As more ions enter the cell, the membrane potential continues to rise. The process continues until all of the ion channels are open, causing a rapid increase in the membrane potential that then triggers the decrease in the membrane potential. The depolarizing is caused by the closing of the ion channels that prevent sodium ions from entering the neuron, and they are then actively transported out of the cell. Potassium channels are then activated, and there is an outward flow of potassium ions, returning the electrochemical gradient to the resting potential. After an action potential has occurred, there is a transient negative shift, called the afterhyperpolarization or refractory period, due to additional potassium currents. This is the mechanism that prevents an action potential from traveling back the way it just came.<ref name="Alberts 2009" /><ref name=":4">{{cite journal|last=Barnett|first=MW|author2=Larkman, PM|title=The action potential.|journal=Practical Neurology|date=Jun 2007|volume=7|issue=3|pages=192–7|pmid=17515599}}</ref>

Another important feature of dendrites, endowed by their active voltage gated conductance, is their ability to send action potentials back into the dendritic arbor. Known as [[Neural backpropagation|back-propagating]] action potentials, these signals depolarize the dendritic arbor and provide a crucial component toward synapse modulation and [[long-term potentiation]]. Furthermore, a train of back-propagating action potentials artificially generated at the soma can induce a calcium action potential (a [[dendritic spike]]) at the dendritic initiation zone in certain types of neurons.{{citation needed|date=June 2015}}

Another important feature of dendrites, endowed by their active voltage gated conductance, is their ability to send action potentials back into the dendritic arbor. Known as [[Neural backpropagation|back-propagating]] action potentials, these signals depolarize the dendritic arbor and provide a crucial component toward synapse modulation and [[long-term potentiation]]. Furthermore, a train of back-propagating action potentials artificially generated at the soma can induce a calcium action potential (a [[dendritic spike]]) at the dendritic initiation zone in certain types of neurons.{{citation needed|date=June 2015}}

==Plasticity 可塑性==

 

==Plasticity==

Dendrites themselves appear to be capable of [[synaptic plasticity|plastic changes]] during the adult life of animals, including invertebrates. Neuronal dendrites have various compartments known as functional units that are able to compute incoming stimuli. These functional units are involved in processing input and are composed of the subdomains of dendrites such as spines, branches, or groupings of branches. Therefore, plasticity that leads to changes in the dendrite structure will affect communication and processing in the cell. During development, dendrite morphology is shaped by intrinsic programs within the cell's genome and extrinsic factors such as signals from other cells. But in adult life, extrinsic signals become more influential and cause more significant changes in dendrite structure compared to intrinsic signals during development. In females, the dendritic structure can change as a result of physiological conditions induced by hormones during periods such as pregnancy, lactation, and following the estrous cycle. This is particularly visible in pyramidal cells of the CA1 region of the hippocampus, where the density of dendrites can vary up to 30%.<ref name=Tavosanis />

Dendrites themselves appear to be capable of [[synaptic plasticity|plastic changes]] during the adult life of animals, including invertebrates. Neuronal dendrites have various compartments known as functional units that are able to compute incoming stimuli. These functional units are involved in processing input and are composed of the subdomains of dendrites such as spines, branches, or groupings of branches. Therefore, plasticity that leads to changes in the dendrite structure will affect communication and processing in the cell. During development, dendrite morphology is shaped by intrinsic programs within the cell's genome and extrinsic factors such as signals from other cells. But in adult life, extrinsic signals become more influential and cause more significant changes in dendrite structure compared to intrinsic signals during development. In females, the dendritic structure can change as a result of physiological conditions induced by hormones during periods such as pregnancy, lactation, and following the estrous cycle. This is particularly visible in pyramidal cells of the CA1 region of the hippocampus, where the density of dendrites can vary up to 30%.<ref name=Tavosanis />

Dendrites themselves appear to be capable of plastic changes during the adult life of animals, including invertebrates. Neuronal dendrites have various compartments known as functional units that are able to compute incoming stimuli. These functional units are involved in processing input and are composed of the subdomains of dendrites such as spines, branches, or groupings of branches. Therefore, plasticity that leads to changes in the dendrite structure will affect communication and processing in the cell. During development, dendrite morphology is shaped by intrinsic programs within the cell's genome and extrinsic factors such as signals from other cells. But in adult life, extrinsic signals become more influential and cause more significant changes in dendrite structure compared to intrinsic signals during development. In females, the dendritic structure can change as a result of physiological conditions induced by hormones during periods such as pregnancy, lactation, and following the estrous cycle. This is particularly visible in pyramidal cells of the CA1 region of the hippocampus, where the density of dendrites can vary up to 30%.

树突在动物包括无脊椎动物的成年生命阶段似乎能够发生可塑性变化。神经元树突有许多被称为功能单元的区域，它们能够对传入的刺激进行计算。这些功能单元参与处理的输入，由树突的子域，如树突棘、分支或分支组组成。因此，引起树突结构变化的可塑性将影响细胞的通信和处理。在发育过程中，树突形态是由细胞基因组编码的内在程序和（来自其他细胞的信号）外在因子塑造的。但在成年阶段，相比于发育阶段，外源信号相比于内源信号，对树突结构的影响更为显著。在女性，树突结构可以因激素诱导的生理状态如怀孕、哺乳、动情周期期间而改变。这在海马 CA1 区的锥体细胞中尤其明显，起树突密度的变化可达30% <ref name="Tavosanis" />。

 

在动物包括无脊椎动物的成年生活中，树突本身似乎能够发生可塑性变化。神经元树突有许多被称为功能单元的区域，它们能够计算传入的刺激。这些功能单元参与处理输入，并由树突的子域组成，如棘、分支或分支组。因此，引起枝晶结构变化的可塑性将影响细胞内的通讯和加工。在发育过程中，树突形态是由细胞基因组内的内在程序和外在因素(如来自其他细胞的信号)形成的。但在成人生活中，外源性信号的影响更大，与内源性信号相比，外源性信号对树突结构的影响更为显著。在女性，树枝状结构可以改变的生理条件诱导的时期，如怀孕，哺乳，以及随后的发情周期。这在海马 ca1区的锥体细胞中特别明显，在那里树突的密度可以高达30% 。

==Notes==

==Notes==